The role of low-frequency electromagnetic fields (EMF) as an environmental agent that contributes to the carcinogenic process has been speculated about, but not proven. Some epidemiological studies suggest that EMF exposure may be linked to brain tumors, leukemias, and breast cancer in some populations. It has been postulated that EMF inhibits the production of melatonin by the pineal gland. Melatonin has been shown to reduce the incidence of carcinogen-induced mammary tumors in rats. We investigated whether melatonin had an anti-proliferative effect on the estrogen-induced proliferation of two estrogen responsive cancer cell lines. While melaton- in had a modest inhibitory effect on the growth of the cells in the absence of estrogen, melatonin had no effect in inhibiting the estrogen-induced proliferation. In addition, melatonin can act as an oxygen radical scavenger. We examined whether melatonin protected cells from cell death induced by high oxygen radicals following hydrogen peroxide treatment. At very high concentrations of melatonin, some of the cells were rescued (20-30%), however, at physiological levels, melatonin had no effect on hydrogen-peroxide induced cell death. This data indicates that melatonin acts directly as an anti-oxidant and does not stimulate anti-oxidant defenses such as the induction of glutathione. Currently we are establishing a new technology, analysis of cDNA microarrays, to allow for sensitive gene expression analysis. We intend to use this technology to compare the gene expression patterns of cells prior and post exposure to EMF to determine what gene/signaling pathways are specifically inhibited/ induced by EMF. This analysis should provide valuable information on the cellular effects of EMF exposure and may allow more reasonable models that implicate EMF as a carcinogen to be developed. This will be the final year for this project.
